ORIGINAL RESEARCH
LI Lili, FANG Pinyan, TANG Jia, ZHANG Jiwang, LIU Bing, CHEN Mengyu, FAN Lijuan
Objective To investigate the association between the pericoronary adipose tissue fat attenuation index (FAI) surrounding culprit plaques in acute coronary syndrome (ACS) and plaque characteristics, and to assess its value in predicting culprit plaques. Methods This retrospective study enrolled 50 patients diagnosed with ACS (ACS group) and 40 asymptomatic individuals with coronary atherosclerosis who underwent coronary computed tomography angiography (CCTA) during the same period (control group). Clinical and imaging data were analyzed. In the ACS group, plaques were classified as culprit or non-culprit plaques. Based on the number of high-risk features, plaques were further categorized as non-high-risk or high-risk. FAI surrounding plaques was measured using predefined default (-190 to -30 HU) and wide (-190 to 20 HU) attenuation thresholds. Student’s t-test, one-way ANOVA, and chi-square test were used to compare FAI values of plaques with different characteristics and degrees of stenosis between and within groups; the plaque characteristics, stenosis severity, and FAI among culprit plaques, non-culprit plaques, and control group plaques; the high-risk features between culprit and non-culprit plaques; and the FAI values between high-risk and non-high-risk plaques. Multivariable logistic regression analysis was performed to identify independent predictors of culprit plaques. Receiver operating characteristic (ROC) curve analysis was used to evaluate the predictive performance of individual and combined factors for culprit plaques. The DeLong test was used to compare the differences in the area under the curve (AUC) among individual and combined factors. Results The FAI measured with the wide threshold was significantly higher than that measured with the default threshold for culprit plaques, non-culprit plaques, and control group plaques (all P<0.05). Under both thresholds, the FAI of culprit plaques was significantly greater than that of non-culprit plaques and control plaques (all P<0.05). Among the culprit plaques, 64% were classified as high-risk plaques, and these also showed high proportions of mixed plaque morphology, severe stenosis, and occlusion (52%, 76%, and 12%, respectively). In the ACS group, the FAI surrounding calcified plaques was lower than that surrounding non-calcified and mixed plaques (P<0.05). The FAI was significantly higher around plaques causing severe stenosis or occlusion (P<0.05), and higher around high-risk plaques compared to non-high-risk plaques (P<0.05). Multivariable logistic regression analysis indicated that stenosis severity ≥ moderate, higher default threshold FAI, and a greater number of high-risk plaque features were independent predictors of culprit plaques. The combination of default threshold FAI, stenosis severity, and high-risk features yielded the highest predictive performance (AUC=0.981). DeLong test analysis showed that the AUCs of models combining default threshold FAI with other factors were significantly higher than those of any single factor alone (all P<0.05). Conclusion The FAI surrounding ACS plaques can partially reflect plaque inflammation and vulnerability. Combining default threshold FAI with stenosis severity and high-risk features improves diagnostic performance in identifying culprit plaques.